This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Recent studies suggest that protein kinase M zeta (PKM[unreadable]) becomes persistently active following learning and may support synaptic activity underlying the permanent storage of long-term memories. If this is the case, inhibiting PKM[unreadable] in the amygdala should permanently erase fearful long-term memories. The work over the last year tested whether PKM[unreadable] inhibition in the amygdala permanently disrupts fear memory by assessing memory at various intervals after PKM[unreadable] blockade. Although the expression of fear memory was disrupted when the inhibitor was applied shortly before testing, it had no effect when rats were tested with longer retention intervals. These results suggest that PKM[unreadable] inhibition does not erase memory, but temporarily disrupts expression of memory. The long-term goal of the work in this proposal is to reach a better understanding of the fundamental issue of how memories are stored in the brain. The work in this project is potentially very useful in coming to a full understanding of how various organic amnesias and psychopathologies develop and persist.